DOI: 10.1093/eurheartj/ehag785.2026 ISSN: 0195-668X

Clinical phenotypes and timing of recurrence in spontaneous coronary artery dissection: insights from a Japanese multicenter registry

N Tamura, K Kato, K Tateishi, Y Saito, Y Kobayashi

Abstract

Background

Recurrent spontaneous coronary artery dissection (SCAD) has been reported in 10–30% of patients, yet the temporal patterns and clinical phenotypes of recurrence remain incompletely characterized. Most existing data originate from Western cohorts, and recurrence patterns in Asian populations are not well defined.

Purpose

To characterize the incidence, timing, and clinical phenotypes of SCAD recurrence in a Japanese multicenter registry.

Methods

This multicenter registry included 175 consecutive patients with SCAD enrolled at 15 participating centers in Japan between 2021 and 2025. Recurrent SCAD was defined as either: (1) a de novo lesion in a different coronary segment, (2) extension of the index SCAD lesion, or (3) unknown. Clinical characteristics, timing of recurrence, and discharge medications were evaluated descriptively.

Results

Among 175 patients (84.6% female; mean age 51.6 ± 10.0 years), 13 patients (7.4%) experienced recurrent SCAD. Recurrence patterns were classified as follows: de novo lesions in 6 patients (3.4%), extension of the index SCAD segment in 5 patients (2.9%), and unknown in 2 patients. A marked temporal difference was observed between recurrence phenotypes. Patients with de novo recurrence developed new lesions at a median of 939 [305–1564] days after the index event, representing late recurrence occurring years after initial presentation. In contrast, extension-type recurrence occurred at a median of 2 [0–3] days, and all cases developed during the index hospitalization, suggesting acute-phase lesion instability rather than late recurrence (Figure). Among patients with extension-type recurrence, escalation of antiplatelet therapy was frequently performed. In patients with de novo recurrence, discharge medications included renin–angiotensin–aldosterone inhibitors (83%), β-blockers (33%), calcium channel blockers (33%), and single antiplatelet therapy (83%). No significant association was observed between β-blocker therapy and recurrence in this cohort. No patients were clinically diagnosed with fibromuscular dysplasia.

Conclusions

In this Japanese multicenter registry, SCAD recurrence was less frequent than previously reported in Western cohorts and demonstrated two distinct temporal phenotypes: acute extension during the index hospitalization and late de novo recurrence years after the initial event. These findings suggest potential pathophysiological and ethnic differences in recurrence patterns and may have implications for surveillance strategies following SCAD.Figure

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